Author + information
- Received March 18, 1996
- Revision received June 27, 1996
- Accepted July 1, 1996
- Published online November 1, 1996.
- Andrew L. Clark, MD, MRCP**,
- Philip A. Poole-Wilson, MD, FRCP and
- Andrew J.S. Coats, DM, FRCP
- ↵**Address for correspondence: Dr. Andrew L. Clark, Level 4 Cardiology, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, Scotland, United Kingdom.
The symptoms of chronic heart failure (CHF) are predominantly shortness of breath and fatigue during exercise and reduced exercise capacity. Disturbances of central hemodynamic function are no longer considered to be the major determinants of exercise capacity. The two symptoms of fatigue and breathlessness are often considered in isolation. A pulmonary abnormality is usually considered to be the cause of abnormal ventilation, and increased dead space ventilation has come to be accepted as a major cause of the increased ventilation relative to carbon dioxide production seen in CHF. Rather than decreased skeletal muscle perfusion, an intrinsic muscle abnormality is considered to be responsible for fatigue. Another abnormality seen in CHF is persistent sympathetic nervous system activation, which is difficult to explain on the basis of baroreflex activation. There is increasing evidence for the importance of skeletal muscle ergoreceptors or metaboreceptors in CHF. These receptors are sensitive to work performed, and activation results in increased ventilation and sympathetic activation. The ergoreflex appears to be greatly enhanced in CHF. We put forward the “muscle hypothesis” as an explanation for many of the pathophysiologic events in CHF. Impaired skeletal muscle function results in ergoreflex activation. In turn, this causes increased ventilation, thus linking the symptoms of breathlessness and fatigue. Furthermore, ergoreflex stimulation may be responsible for persistent sympathetic activation.
This study was supported by the Robert Luff Foundation (Dr. Clark), the Viscount Royston Trust (Dr. Coats) and the British Heart Foundation (Drs. Coats and Poole-Wilson), London, England, United Kingdom.
- Received March 18, 1996.
- Revision received June 27, 1996.
- Accepted July 1, 1996.
- American College of Cardiology